It is observed that the increase in blood-brain barrier (BBB) permeability (BBBP) is associated with ischemic stroke and thought to trigger neuronal damage and deteriorate ischemic infarction, even though there is no experimental proof. Here, we investigated the effect of BBBP increase on brain damage, using a combination of photochemically-induced thrombotic brain damage (PIT-BD) model, a focal brain ischemic model, and transient bilateral carotid artery occlusion model (CAO, a whole brain ischemic model), in mice. In PIT-BD, BBBP increased in the region surrounding the ischemic damage from 4 h till 24 h with a peak at 8 h. On day 4, the damaged did not expand to the region with BBBP increase in mice with PIT-BD alone or with 30 min CAO at 1 h before PIT-BD, but expanded in mice with 30 min CAO at 3.5 h after PIT-BD. This expansion was paralleled with the increase in the number of apoptotic cells. These findings indicate that increase in BBBP does not cause direct neuronal death, but it facilitates ischemic neuronal loss, which was attributed, at least partially, to acceleration of apoptotic cell death.

Repair of brain damage size and recovery of neurological dysfunction after ischemic stroke are different between strains in mice: Evaluation using a novel ischemic stroke model.

There is an urgent need to address the shortage of animal protein due to food shortages caused by the global population growth. Crickets contain an abundance of proteins in their exoskeleton and muscles and have attracted attention as a new protein source; however, their safety as a food source has not been confirmed. We evaluated the toxicity of the House cricket (Acheta domesticus), on cells and mammals. In genotoxicity in vitro, cricket powder was added to Chinese hamster lung CHL-IU cells at concentrations of 5,000 μg/mL, and the rate of chromosomal aberrations was assessed. In genotoxicity in vivo, mice were orally administered up to 2,000 mg/kg of cricket powder for 2 days. In both tests, cricket powder did not show any toxic effect. A repeated oral toxicity study was performed administering up to 3,000 mg/kg of cricket powder or control (saline) for 14 or 90 consecutive days and measuring body weight changes, blood biochemistry, blood properties, and organ weights. In each time course, there were no differences in there parameters between the control and cricket powder treated groups. These results suggest that House crickets (≤3,000 mg/kg) are not toxic to cells and organisms.

BackgroundSince previously established models of pulmonary embolism showed a large variability in the degree of ischemia, it is difficult to assess the pathophysiological response in the lung after embolization. Here, we established a model of pulmonary embolism by certain amount of relatively small thrombi, in which the degree of ischemia was reproducible.MethodsThrombi with a maximum diameter of 100 μm or 500 μm were administered intravenously under anesthesia, and the survival ratio at 4 hours was evaluated. The location of thrombi in the lung was visualized by administration of fluorescent-labeled thrombus, and the hemodynamics of the lung after administration of thrombi was evaluated. CT angiography was also performed to evaluate the ratio of the embolized vessels. In addition, cytokine mRNAs was quantified 4 hours in embolized lung. Immunohistochemical analysis for interleukin (IL)-6 and CD68 as a marker of macrophages were also performed.ResultsIt was found that mice with 100 μm clots, but not with 500 μm clots, showed a dose-dependence of survival between 2.3 μL/g and 3.0 μL/g at 4 hours from embolization induction. In mice treated with 2.5 μL/g of 100 μm thrombus, thrombi were located in the peripheral region of the lung, which was consistent with the disruption of blood circulation the peripheral region. In addition, about 60% of the vessels with a diameter of less than 100 μm were occluded in these mice. In the lungs after 4 hours of embolization, IL-6 mRNA and tumor necrosis factor (TNF)-α mRNA were significantly higher and lower than control lungs. IL-6 was expressed in CD68-positive macrophages in both embolized and control lungs after 4 hours of embolization, and the number of each positive cells were comparable in both embolized and control lungs.ConclusionsThese results show that the pulmonary embolization model induced by a certain amount of small thrombus is useful for evaluating the pathological responses in the embolized lung. Furthermore, it was found that IL-6 expression was increased in macrophages in the embolized lung, indicating that inflammatory responses may contribute to the pathogenesis of pulmonary embolism.